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Department of Nutrition, School of Public Health and * Department of Nutrition and Dietetics, School of Allied Health, Loma Linda University, Loma Linda, California.
2To whom correspondence should be addressed. E-mail: jsabate{at}sph.llu.edu.
| ABSTRACT |
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KEY WORDS: lipids lipoproteins fatty acids cardiovascular diseases
| INTRODUCTION |
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There is epidemiologic evidence that frequent consumption of nuts
protects both men and women from CHD (5
6
7)
. Previously we
showed that polyunsaturated fatty acid (PUFA)-rich walnuts reduced
serum total and LDL cholesterol in healthy men compared with the Step I
diet (8)
or a Mediterranean diet (9)
.
Recently, the Scientific Advisory of the American Heart Association
reported (10)
that high monounsaturated fatty acid (MUFA)
diets tend to raise HDL and lower triacylglycerol concentration
compared with low fat, carbohydrate-rich, cholesterol-lowering
diets (11
,12)
. In keeping with this evidence, we chose to
study the effect of MUFA-rich pecans on blood lipids. Pecans are
considered to be the traditional tree nut in the United States. In
addition to being a rich source of MUFA, the unique nonfat component of
pecans may also have a role in favorably modifying the blood lipid
profile and potentially other cardiovascular risk factors. Thus, the
objective of this controlled feeding study was to investigate the
effect of pecans on blood lipids and lipoproteins in healthy men and
women compared with the Step I diet.
| SUBJECTS AND METHODS |
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Healthy men and women volunteers from Loma Linda University and
surrounding communities were selected at the completion of a multiphase
screening process that included a questionnaire, group meeting,
face-to-face interview with a senior investigator and an assessment of
serum cholesterol and triacylglycerol concentrations. Subjects with
serum cholesterol below the 15th or above the 80th percentile for their
age, race and gender (13)
and triacylglycerol >2.26
mmol/L (200 mg/dL) were excluded from the study. Also excluded were
subjects who ate nuts (>2 times/wk), had food allergies, smoked
cigarettes, drank caffeinated beverages (
3 times/d) or alcohol (more
often than on a rare social occasion), had a history of CHD or other
metabolic diseases, took medication that interfered with lipid
metabolism or had a body mass index >30 kg/m2. Women who
had started hormone replacement within 5 y of entry into the study
and those with irregular menses were also excluded.
Statistical power calculations indicated that to detect mean differences of 0.26 mmol/L (10 mg/dL) for total and LDL cholesterol, 22 participants would have to complete the two treatment periods (statistic, 0.05; power >0.9) of this crossover design. Of the 24 subjects who were randomly assigned to groups, 23 (11 Caucasians, 6 Asians, 4 Hispanics and 2 African-Americans) successfully completed the study. There were 9 women and 14 men in the age range of 2555 y. The body weight and baseline serum cholesterol of the subjects were 74.4 ± 16.7 kg and 4.64 ± 0.83 mmol/L [179.4 ± 32.2 mg/dL], respectively. The study protocol was approved by the Institutional Review Board of the University; all interested subjects signed the informed consent form and were offered a cash incentive of $200 upon successful completion of the study.
Study and diet design.
The first 2 wk of this single-blind, crossover study comprised a
run-in phase in which subjects were fed a typical American diet
(34% energy from total and 15% from saturated fat). The subjects were
randomly assigned after stratification based on two categories of age,
gender and screening values of serum cholesterol, into either the Step
I diet or the pecan-enriched diet for the first 4 wk. The groups
then reversed their diet intervention and continued for another 4 wk.
Given that lipoprotein values stabilize in <4 wk of a diet
intervention (14)
, and based on our previous studies that
showed no carry-over effects with walnuts (8
,9)
, we
did not include a washout period between the two diet periods in this
study. The diets were isoenergetic, but the percentage of energy from
fat was higher in the pecan (39.6%) than in the Step I diet (28.3%).
Pecans did not replace a given food or fat in the Step I diet, but a
portion of the entire diet. This was accomplished by reducing the
portion size of all items on the menu of the Step I diet by one fifth
(i.e., total energy was reduced by 20%) to accommodate the pecans,
which were served plain, in salads, gravies, shakes and as toppings.
The amount of pecans consumed daily by the subjects per 10,032 kJ (2400
kcal) was 72 g (2.5 oz).
Meal service and quality control.
All meals were prepared in the University Metabolic Kitchen and each food accurately weighed to the nearest gram by trained weighers. Subjects ate breakfast and dinner, Sunday through Friday, in the Metabolic Kitchen dining facility, and all lunches and Saturday meals were packed for carry out. A total of nine different daily menus of commonly consumed foods were prepared using standardized recipes; menus were used in rotation to increase variety.
For subjects to maintain constant body weight during the study, energy intake had to be adjusted periodically. Frequent monitoring of body weight throughout the study and subjective feelings of hunger expressed by participants were used in making the necessary adjustments in energy intake. The energy intake used in this study ranged from 8368 (2000 kcal) to 15,062 kJ (3600 kcal) with 1674 kJ (400 kcal) increments. Homogenized samples of both diets were collected on 18 randomly selected days covering both diet periods. Samples were mixed and analyzed for macronutrients and fatty acid composition (Covance Laboratories, Madison, WI).
Compliance.
Subjects were required to consume all meals served in the Metabolic Kitchen and were not allowed to consume nonstudy foods or beverages except water. They were required to maintain the same lifestyle activities as reported at the time of the screening interview. Subjects were asked to record any deviations from this "norm" in a diary, which was reviewed frequently by an investigator, one of whom was always present at meal times to interact with the subjects. Dietary compliance was also assessed by measuring plasma fatty acids (UC Davis Nutrition laboratory) at the end of each diet intervention.
Laboratory measurements.
Blood was drawn from fasting subjects on two alternate days at the end of the run-in phase and the end of the two diet periods. All samples were processed immediately (Smith-Kline Beecham, Loma Linda, CA) and serum aliquots shipped to the Nutritional Assessment Core of the University of California, Davis (NIH Clinical Nutrition Research Unit, NIDDK 35747) for analyses. Serum total cholesterol, LDL cholesterol, HDL cholesterol and triacylglycerol were determined by enzymatic assays using the 550 Express Chemistry Analyzer (Bayer, Tarrytown, NY). HDL cholesterol was determined after anionic precipitation of apolipoprotein (apo) B-containing lipoproteins. Apo A1 and B were measured by rate immunonephelometry (Beckman Coulter, Brea, CA). Lipoprotein(a) [Lp(a)] was determined turbidimetrically (DiaSorin, Stillwater, MN). The diet groupings were not disclosed to the laboratory personnel.
Statistical analysis.
Mean and standard deviations are presented for each measurement.
Differences between the pecan-enriched and Step 1 diets were tested
by repeated-measures analysis of variance and covariance; baseline
values or gender were used as covariates. Period and carry-over
effects were evaluated using appropriate interaction terms. Analyses
were performed using SAS software (15)
. Differences were
considered significant at P < 0.05.
| RESULTS |
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We observed a high degree of congruence between the planned and
analyzed diet composition (Table 1
). The percentages of energy from MUFA and PUFA were almost 100%
greater in the pecan-enriched diet than in the Step I diet,
resulting in markedly different PUFA:MUFA:saturated fatty acid (SFA)
ratios in the Step I (6:11:8) and pecan-enriched (11:19:8) diets.
Pecan consumption in the study was 100% because they were consumed
under supervision. We estimated the overall dietary compliance to be
>95% on the basis of supervision by investigators during on-site
meal times, 6 d a week, and by personal diaries kept by subjects.
In addition, the fatty acid composition of the triacylglycerol fraction
of plasma lipids and those of the two diets were consistent. As
expected, plasma triacylglycerol SFA and ratios of SFA to MUFA and SFA
to PUFA were significantly lower when subjects consumed the
pecan-enriched diet compared with the Step I diet (Table 2
). This was expected given the higher percentage of energy from oleic
acid in the pecan-enriched diet (18.5%) compared with the Step I
diet (10.5%).
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Serum lipid, lipoprotein and apolipoprotein concentrations at the end
of each diet period as well as the differences of effect between
dietary interventions are given in Table 3
. No carry-over effect was observed between the dietary periods.
Serum total and LDL cholesterol were lower by 0.32 mmol/L (12.3 mg/dL),
whereas HDL cholesterol was greater by 0.06 mmol/L (2.5 mg/dL) when
subjects consumed the pecan-enriched diet compared with the Step I
diet. This corresponded to 6.7 and 10.4% decreases in total and LDL
cholesterol, respectively, and a 5.6% increase in HDL cholesterol when
subject consumed the pecan-enriched diet beyond the effects of the
Step I diet. The LDL cholesterol to HDL cholesterol ratio was lower by
0.44 when subjects consumed the pecan-enriched diet compared with
the Step I diet. Plasma triacylglycerol, apo B and Lp(a) concentrations
were significantly lower by 11.1% [0.14 mmol/L (12.7 mg/dL)], 11.6%
(0.10 g/L), 15.1% (0.04 g/L) respectively, and apo A1 significantly
greater by 2.2% (0.03 g/L) when subjects consumed the
pecan-enriched compared with the Step I diet. All differences were
significant.
|
Figure 1
depicts the effectiveness of the pecan-enriched diet compared with
the Step I diet by comparing the changes in serum lipid concentrations
due to the two test diets to concentrations at the end of the
run-in phase (baseline) when subjects consumed a typical American
diet. As expected, the Step I diet lowered total and LDL cholesterol
compared with the American diet. However, the pecan-enriched diet
significantly lowered serum total and LDL cholesterol beyond that of
the Step I diet. Furthermore, the pecan-enriched diet prevented the
decrease in HDL cholesterol and the increase in triacylglycerol
observed with the Step I diet and significantly decreased apo B.
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| DISCUSSION |
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Serum apo B concentrations decreased and apo A1 concentrations
increased when subjects consumed the pecan-enriched diet. These
changes paralleled those observed with LDL and HDL cholesterol,
respectively. A decrease in the synthesis of VLDL, the primary carrier
of hepatic triacylglycerol, and an increase in its catabolism may be
the cause of the decrease in plasma triacylglycerol (18)
.
The lowering of triacylglycerol by other MUFA-rich foods has
previously been demonstrated (11
,19)
. The increase in HDL
cholesterol due to the pecan-enriched diet was expected
(12)
given the higher percentage of fat contributed by the
pecans. Also, the concomitant increase in apo A1, which stimulates
cholesterol uptake by HDL, may explain in part the increase in HDL
cholesterol observed when subjects consumed the pecan-enriched
diet.
Changes in blood lipids were calculated by predictive equations that
included changes in dietary fatty acid, cholesterol and total fat
intake (20
21
22
23)
. These models estimated changes in serum
total cholesterol ranging from 0.11 to -0.20 mmol/L (4.3 to -7.7
mg/dL) and in LDL cholesterol ranging from -0.11 to -0.25 mmol/L
(-4.3 to -9.7 mg/dL). These values are much less than the mean
decrease of 0.32 mmol/L (12.4 mg/dL) observed for both total and LDL
cholesterol, and mainly outside their corresponding 95% confidence
intervals. The lipid component of pecans contributed to the observed
effects on blood lipids, but cholesterol was lowered more than the
decrease estimated from differences in the fat content of the two
diets. One third of pecans by weight is nonfat, and includes dietary
fiber and proteins with a low ratio of lysine to arginine. Both fiber
and a low ratio of lysine to arginine lower cholesterol
(24
25
26)
. In addition to the traditional nutrients, the
phytochemicals present in pecans may be quantified and explored in the
future for their potential role in reducing some of the risk factors of
CHD. Thus, the nonfat matrix of pecans may also contribute to the
lipid-lowering effects observed in this study.
The beneficial changes in serum Lp(a), an independent risk factor for
CHD (27)
and the lipoprotein that is considered to be
least affected by diet, are interesting. We and others
(3
,9)
have shown that Step I and Step II diets raise serum
Lp(a) concentrations. In this study, serum Lp(a) was significantly
lower in both men and women when they consumed the pecan-enriched
diet. Walnuts (9)
and fish oil (28)
, two
excellent sources of PUFA of the (n-3) family, have both been shown to
lower Lp(a) concentrations in healthy and hypercholesterolemic men.
Given that walnuts and pecans, one rich in PUFA and the other in MUFA,
both lowered Lp(a) suggests that nuts as a family may have some common
component in addition to lipids that influences Lp(a) concentrations.
It has been shown that for every 1% reduction in LDL cholesterol there
is a 1.5% reduction in the incidence of CHD (29)
. In this
study, the 16% decrease in LDL cholesterol in the pecan-enriched
diet compared with the American diet (Fig. 1)
corresponds to a 25%
decrease in CHD risk. Epidemiologic studies (5
6
7)
have
estimated that the percentage of decrease in CHD risk with frequent
consumption of nuts is 4050%. This suggests that the favorable
changes in HDL cholesterol, Lp(a) and triacylglycerol
(30
,31)
observed in the pecan group, and other mechanisms
not determined in this study, may contribute to the cardioprotective
effects of nuts.
Aside from the issue of suboptimal changes in the blood lipid profile,
there is currently a heightened interest in searching for alternatives
to the Step I diet because of difficulties with dietary compliance
(32
,33)
. Part of the challenge in complying with diets
that are lower in total and saturated fat is that they require the
elimination and restriction of foods. A viable alternative is an
approach that relies on incorporating whole foods such as high MUFA
nuts into self-selected diets or prescribed lipid-lowering
diets. Recently, olive oil, a constituent of the Mediterranean diet,
has been recommended as a source of MUFA (4)
. Because it
is a fluid fat, olive oil and other high MUFA oils may be of somewhat
limited use in everyday American cooking. In contrast, pecans and other
high MUFA nuts are perhaps more versatile and easier to incorporate
into different types of diets. This has the potential to improve
dietary compliance in many patients consuming lipid-lowering diets.
In summary, the pecan-enriched diet favorably altered the blood
lipid profile beyond that observed with the Step I diet. Because of the
beneficial effects of nuts on several biomarkers of CHD risk and on the
basis of previously reported epidemiologic evidence that showed a
lowering of CHD risk with frequent consumption of nuts
(5
6
7)
, it seems prudent to recommend inclusion of high
MUFA nuts in cholesterol-lowering diets, or as a start, in
self-selected diets.
| ACKNOWLEDGMENTS |
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| FOOTNOTES |
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3 Abbreviations used: apo, apolipoprotein; CHD,
coronary heart disease; Lp(a), lipoprotein(a); MUFA, monounsaturated
fatty acids; PUFA, polyunsaturated fatty acids; SFA, saturated fatty
acids. ![]()
Manuscript received March 5, 2001. Initial review completed April 20, 2001. Revision accepted June 3, 2001.
| LITERATURE CITED |
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1. Davis C. E., Rifkind B. M., Brenner H. & Gordon D. J. (1990) A single cholesterol measurement underestimates the risk of coronary heart disease: an empirical example from the Lipid Research Clinics mortality follow-up study. J. Am. Med. Assoc. 264:3044-3046.[Abstract]
2. Stone N. J., Nicolosi R. J., Kris-Etherton P., Ernst N. D., Krauss R. M. & Winston M. (1996) Summary of the Scientific Conference on the Efficacy of Hypocholesterolemic Dietary Interventions. Circulation 94:3388-3391.[Medline]
3.
Ginsberg H. N., Kris-Etherton P., Dennis B., Elmer P. J., Ershow A., Lefevre M., Pearson T., Roheim P., Ramakrishnan R., Reed R., Stewart K., Stewart P., Phillips K. & Anderson N. (1998) Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1. Arterioscler. Thromb. Vasc. Biol. 18:441-449.
4. Katan M. B., Grundy S. M. & Willett W. C. (1997) Should a low-fat, high-carbohydrate diet be recommended for everyone? Beyond low-fat diets. N. Engl. J. Med. 337:563-566.
5. Fraser G. E., Sabate J., Beeson W. L. & Strahan T. M. (1992) A possible protective effect of nut consumption on risk of coronary heart disease: the Adventist Health Study. Arch. Intern. Med. 152:1416-1424.[Abstract]
6.
Kushi L. H., Folsom A. R., Prineas R. J., Mink P. J., Wu Y. & Bostick R. M. (1996) Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women. N. Engl. J. Med. 334:1156-1162.
7.
Hu F. B., Stampfer M. J., Manson J. E., Rimm E. B., Colditz G. A., Rosner B. A., Speizer F. E., Hennekens C. H. & Willett W. C. (1998) Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. Br. Med. J. 317:1341-1345.
8.
Sabate J., Fraser G. E., Burke K., Knutsen S. F., Bennett H. & Lindsted K. D. (1993) Effects of walnuts on serum lipid concentrations and blood pressure in normal men. N. Engl. J. Med. 328:603-607.
9. Zambon D., Sabate J., Munoz S., Campero B., Casals E., Merlos M., Laguna J. C. & Ros E. (2000) Substituting walnuts for monounsaturated fat improves the serum lipid profile of hypercholesterolic men and women. Ann. Intern. Med. 7:538-546.
10. Kris-Etherton P. (1999) Monounsaturated fatty acids and risk of cardiovascular disease. Circulation 100:1253-1258.[Medline]
11. Grundy S. M. (1986) Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. N. Engl. J. Med. 314:745-748.[Abstract]
12. Mensink R. P. & Katan M. B. (1987) Effect of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women. Lancet 1:122-125.[Medline]
13. National Cholesterol Education Program (1993) Second report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II), NIH Publication no. 933095 1993 National Cholesterol Education Program, National Institutes of Health, National Heart, Lung and Blood Institute , Bethesda, MD .
14.
Kris-Etherton P. M. & Dietschy J. (1997) Design criteria for studies examining individual fatty acid effects on cardiovascular disease risk factors: human and animal studies. Am. J. Clin. Nutr. 65(suppl.):1590S-1596S.
15. The GLM Procedure. 4th ed. SAS/STAT Users Guide, Version 6 2:891-996 SAS Institute Cary, NC .
16. Morgan W. A. & Clayshulte B. J. (2000) Pecans lower low-density lipoprotein cholesterol in people with normal lipid concentrations. J. Am. Diet. Assoc. 100:312-318.[Medline]
17.
Connor W. E. & Connor S. L. (1997) Should a low-fat, high-carbohydrate diet be recommended for everyone? The case for a low-fat high-carbohydrate diet. N. Engl. J. Med. 337:562-563.
18. Roche H. M., Zampelas A., Knapper J. M., Webb D., Brooks C., Jackson K. G., Wright J. W., Gould B. J., Kafatos A., Gibney M. J. & Williams C. M. (1998) Effect of long-term olive oil dietary intervention on postprandial triacylglycerol and factor VII metabolism. Am. J. Clin. Nutr. 68:552-560.[Abstract]
19.
Kris-Etherton P. M., Pearson T. A., Wan Y, Hargrove R. L., Moriarty K., Fishell V. & Etherton T. D. (1999) High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am. J. Clin. Nutr. 70:1009-1015.
20. Keys A., Anderson J. T. & Grande F. (1965) Serum cholesterol response to changes in the diet IV. Particular saturated fatty acids in the diet. Metabolism 14:776-787.
21. Mensink R. P. & Katan M. B. (1992) Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler. Thromb 12:911-913.[Abstract]
22.
Yu S., Derr J., Etherton T. D. & Kris-Etherton P. M. (1995) Plasma cholesterol-predictive equations demonstrate that stearic acid is neutral and monounsaturated fatty acids are hypocholesterolemic. Am. J. Clin. Nutr. 61:1129-1139.
23.
Clarke R., Frost C., Collins R., Appleby P. & Peto R. (1997) Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. Br. Med. J. 314:112-117.
24. Sabaté J., Bell H.E.T. & Fraser G. E. (1996) Nut consumption and coronary heart disease risk. Spiller G. A. eds. Handbook of Lipids in Human Nutrition 1996:145-151 CRC Press Boca Raton, FL. .
25.
Anderson J. W., Smith B. M. & Gustafson N. J. (1994) Health benefits and practical aspects of high-fiber diets. Am. J. Clin. Nutr. 59(suppl.):1242S-1247S.
26.
Anderson J. W., Johnstone B. M. & Cook-Newell M. E. (1995) Meta-analysis of the effects of soy protein intake on serum lipids. N. Engl. J. Med. 333:276-282.
27. Orth-Gomer K., Mittleman M. A., Schenck-Gustafsson K., Wamala S. P., Eriksson M., Belkic K., Kirkeeide R., Svane B. & Ryden L. (1997) Lipoprotein(a) as a determinant of coronary heart disease in young women. Circulation 95:329-334.[Medline]
28. Eritsland J., Arnesen H., Berg K., Seljeflot I. & Abdelnoor M. (1995) Serum Lp(a) lipoprotein concentrations in patients with coronary artery disease and the influence of long-term n-3 fatty acid supplementation. Scand. J. Clin. Lab. Investig. 55:295-300.[Medline]
29. National Cholesterol Education Program (1991) Report of the Expert Panel on Population Strategies for Blood Cholesterol Reduction. Circulation 83:2154-2232.[Medline]
30. Criqui M. H. (1998) Triacylglycerol and cardiovascular disease. A focus on clinical trials. Eur. Heart J. 19:A36-A39.
31. Seman L. J., McNamara J. R. & Schaefer E. J. (1999) Lipoprotein(a), homocysteine, and remnant like particles: emerging risk factors. Curr. Opin. Cardiol. 14:186-191.[Medline]
32. Headrick L. A., Speroff T., Pelecanos H. I. & Cebul R. D. (1992) Efforts to improve compliance with the National Cholesterol Education Program guidelines. Results of a randomized controlled trial. Arch. Intern. Med. 152:2385-2387.[Medline]
33. McManus K., Roberts C. & Manson J. E. (1996) Appendix A, Nutrition guidelines for reducing coronary risk. Manson J. E. Ridker P. M. Gaziano J. M. Hennekens C. H. eds. Prevention of Myocardial Infarction 1996:529-540 Oxford University Press New York, NY. .
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